Figure 835

Renal hemodynamic response to mild partial ureteral obstruction. Renal blood flow and the glomerular filtration rate may not change in mild partial ureteral obstruction, despite a significant reduction in glomerular capillary ultrafiltration coefficient (Kf). This is due to the increase in glomerular capillary hydraulic pressure (PGC) caused by a prostaglandin E2-induced reduction of afferent arteriolar resistance (RA) and an angiotensin Il-induced elevation of efferent arteriolar resistance (RE). It is likely that other vasoactive factors, such as thromboxane A2, also play a role, particularly in more severe ureteral obstruction accompanied by reductions in renal blood flow and glomerular filtration rate [46]. PGE2—prostaglandin E2; PGI2—prostaglandin I2; Pt—tubule hydrostatic pressure.

2 h post-obstruction

24 h post-obstruction t N0

HP, t Endothelin t Angiotensin II t TBX A, t N0


(Macrophage infiltration) t RBF (120%) i ^

\ GFR (80%) (Activation of ^ renin-angiotensin)

Unilateral tR.

0 0

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